| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Journal of Clinical Endocrinology & Metabolism, Vol 79, 134-139, Copyright © 1994 by Endocrine Society
ARTICLES |
P Kopp, ET Kimura, S Aeschimann, M Oestreicher, A Tobler, MF Fey and H Studer
Department of Internal Medicine, Inselspital, Bern, Switzerland.
Although somatic mutations have been identified in a subset of thyroid nodules, the pathogenesis of nodules in multinodular goiters remains unclear. Clonal analysis indicates whether a nodule arises from the polyclonal proliferation of a group of cells or forms a clone from a genetically altered cell. Individual thyroid nodules have been shown to be of polyclonal or monoclonal origin. In this study we examined the clonality of several different nodules in patients with multinodular goiters. Clonality was established using the X-chromosomal probe M27 beta, which detects a multiallelic polymorphism at the locus DXS255 in 90% of females. Twenty-five nodules from 9 multinodular goiters were analyzed; 9 nodules were polyclonal, and 16 were monoclonal. Three goiters contained only polyclonal nodules, whereas 3 contained only monoclonal nodules. Polyclonal and monoclonal nodules coexisted in 3 goiters. In 2 goiters, the monoclonal nodules were shown to derive from different progenitor cells. We conclude that polyclonal and monoclonal nodules may coexist in multinodular goiters and that monoclonal nodules can originate from different cells. The coexistence of polyclonal and monoclonal nodules suggests that different pathogenic mechanisms occur simultaneously or that monoclonal nodules emerge secondarily from a polyclonal population due to a growth advantage from a genetically altered cell.
This article has been cited by other articles:
![]() |
K. Krohn, D. Fuhrer, Y. Bayer, M. Eszlinger, V. Brauer, S. Neumann, and R. Paschke Molecular Pathogenesis of Euthyroid and Toxic Multinodular Goiter Endocr. Rev., June 1, 2005; 26(4): 504 - 524. [Abstract] [Full Text] [PDF] |
||||
![]() |
S L Asa My approach to oncocytic tumours of the thyroid J. Clin. Pathol., March 1, 2004; 57(3): 225 - 232. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Jovanovic, B. Delahunt, B. McIver, N. L. Eberhardt, and S. K. G. Grebe Thyroid Gland Clonality Revisited: The Embryonal Patch Size of the Normal Human Thyroid Gland Is Very Large, Suggesting X-Chromosome Inactivation Tumor Clonality Studies of Thyroid Tumors Have to Be Interpreted with Caution J. Clin. Endocrinol. Metab., July 1, 2003; 88(7): 3284 - 3291. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Martins, S. E. Matsuo, K. N. Ebina, M. A. V. Kulcsar, C. U. M. Friguglietti, and E. T. Kimura Galectin-3 Messenger Ribonucleic Acid and Protein Are Expressed in Benign Thyroid Tumors J. Clin. Endocrinol. Metab., October 1, 2002; 87(10): 4806 - 4810. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. G. Kroll Molecular Rearrangements and Morphology in Thyroid Cancer Am. J. Pathol., June 1, 2002; 160(6): 1941 - 1944. [Full Text] [PDF] |
||||
![]() |
K. Krohn and R. Paschke Progress in Understanding the Etiology of Thyroid Autonomy J. Clin. Endocrinol. Metab., July 1, 2001; 86(7): 3336 - 3345. [Full Text] [PDF] |
||||
![]() |
X. Matias-Guiu Mixed Medullary and Follicular Carcinoma of the Thyroid : On the Search for Its Histogenesis Am. J. Pathol., November 1, 1999; 155(5): 1413 - 1418. [Full Text] [PDF] |
||||
![]() |
M. D. Ringel, M. Saji, W. F. Schwindinger, D. Segev, M. A. Zeiger, and M. A. Levine Absence of Activating Mutations of the Genes Encoding the {alpha}-Subunits of G11 and Gq in Thyroid Neoplasia J. Clin. Endocrinol. Metab., February 1, 1998; 83(2): 554 - 559. [Abstract] [Full Text] |
||||
![]() |
L. Duprez, J. Hermans, J. Van Sande, J. E. Dumont, G. Vassart, and J. Parma Two Autonomous Nodules of a Patient with Multinodular Goiter Harbor Different Activating Mutations of the Thyrotropin Receptor Gene J. Clin. Endocrinol. Metab., January 1, 1997; 82(1): 306 - 308. [Full Text] [PDF] |
||||
![]() |
P. Kopp, J. van Sande, J. Parma, L. Duprez, H. Gerber, E. Joss, J. L. Jameson, J. E. Dumont, and G. Vassart Congenital Hyperthyroidism Caused by a Mutation in the Thyrotropin-Receptor Gene N. Engl. J. Med., January 19, 1995; 332(3): 150 - 154. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |